The goal of this work is to understand the membrane aspects of paramyxovirus infections. Paramyxovirus membranes fuse with host cell membranes, after which the virus disassembles and the viral membrane components become distributed in the host membrane. Paramyxovirus membranes behave similarly with liposomes containing gangliosides which act as viral receptors. The occurrence both of membrane fusion and of viral disassembly depend upon the liposomal composition. This model system will be used to study: A. The mechanism of membrane fusion. To see what conditions must be fulfilled for fusion to occur the role of individual liposomal lipids, their distribution, their fluidity and possible requirements for specific domains and lateral phase separations will be determined. B. The details of virus disassembly. The lipid requirements for disassembly are independent of those for fusion since in liposomes of some compositions membrane fusion can occur without viral disassembly. In many cases after disassembly viral glycoproteins form patches in the liposome. The lipid and physical requirements for disassembly with and without patching will be determined. Those liposomes of compositions that allow patching will be fused with labeled virus, and sonicated to produce fragments which will be analyzed for individual viral and liposomal components. This will show the steps of disassembly, and the composition of the fragments should reflect both viral protein-lipid and protein-protein interactions and whether the latter is affected by the lipid composition. C. Viral membrane protein-lipid ineractions. Whether viral proteins preferentially associate with specific lipids will be studied further by determining if specific lipids can be cross-linked to viral proteins by cross-linking reagents. To see if lipid composition can affect the functions of the viral proteins, the neuraminidase, hemagglutinating, and fusion activities of the viral proteins will be assayed in liposomes of different compositions.